After 10 minute global of ischemia in rat brain, a marked increase in abnormal calcium uptake and suppression of protein synthesis in nuclei reticularis of thalamus was observed as early as 6 hours postischemia, followed by a significant increase in abnormal accumulation of calcium at moderately reduced rates of protein synthesis in the ventral thalamic nucleus and inferior colliculus which lasted up to 7 days postischemia. In hippocampal CAl sector, protein synthesis of CAl neurons was severely suppressed until 4 days postischemia, but recovered significantly to subnormal levels of protein synthesis after 7 days postischemia. Metabolic amelioration of hippocampal CAl neurons correlated with their improvement of morphological appearance. Our findings suggest l) that early postischemic calcium accumulation occurring predominantly in GABAergic brain areas appears to reflect the consequences of inhibition failure of GABAergic interneurons which may result in a subsequent 'disinhibition' of interconnected projection areas and the development of remote neuron injury; and 2) that following a phase of chronic neuronal injury, hippocampal CAl neurons are able to recover from an ischemic insult.